The present study demonstrated that sevoflurane post‑conditioning could protect middle cerebral artery occlusion‑induced brain injury rats by inhibiting autophagy and apoptosis, and that its mechanism is related to the TLR4‑NF‑κB signaling pathway.
Western blot assay results showed that expression of Toll-like receptor 4, nuclear factor kappa B, NLRP3, procaspase-1, caspase-1, pro-interleukin-1β, and interleukin-1β were significantly lower in the acacetin group compared with the middle cerebral artery occlusion group.
The infarct volume was significantly reduced and white matter damage was also significantly alleviated in the melatonin group as compared with the MCAO group (P < 0.05), and there were more TLR4<sup>+</sup>, NF-κB<sup>+</sup> and IL-1β<sup>+</sup> cells in the MCAO group compared with the melatonin group (P < 0.01).
The results of the present study suggested that TLR4 may promote the phosphorylation of CRMP2 via the activation of ROCK‑II in MCAO rats, which further characterizes the pathological mechanism of TLR4 in stroke, and that modulation of TLR4 could be a potential target to limit secondary post‑stroke brain damage.
Curcumin in MCAO rats significantly improved brain damage and neurological function by upregulating p-Akt and p-mTOR and downregulating LC3-II/LC3-I, IL-1, TLR4, p-38, and p-p38.
ApTLR#4F and ApTLR#4FT showed a long-lasting protective effect against brain injury induced by middle cerebral artery occlusion (MCAO), an effect that was absent in TLR4-deficient mice.
Using Cy3 labeling, exogenous miR-1906 expression was visualized and shown to enter astrocytes, microglia, and neurons successfully <i>in vivo</i> Supplemental therapeutic miR-1906 resulted in reduced TLR4 expression and improved outcomes after middle cerebral artery occlusion in a mouse model, but its neuroprotective function was TLR4 dependent, suggesting that TLR4 is a major target of miR-1906.
In the present study, the effects of TRPV1 receptor activation and blockade on stroke outcome and gene expression of TLR2 and TLR4 were assessed following permanent middle cerebral artery occlusion in rats.
Using a middle cerebral artery occlusion (MCAO) model, triphenyltetrazolium chloride staining was utilized to measure the infarct volume and brain edema and immunofluorescence staining was used to detect the MCAO-induced TLR4 expression and localization.